Chloramphenicol (C14 has previously been shown to be covalently bound in vivo predominantly to proteins of the liver, bone marrow, and plasma. The present research is being conducted in order to determine the mechanism(s) by which chloramphenicol is activated to metabolites that react with tissue macromolecules. This study will hopefully lead to a better general understanding of the mechanism(s) involved in chloramphenicol-induced bone marrow damage. In addition, it may also lead to an intimate understanding of the chemical reactions between reactive metabolites and biological molecules. Such interactions appear to be involved in the hepatotoxicity, and carcinogenicity induced by several chemical agents. Similar interactions may also be involved in the development of blood dyscrasias, such as chloramphenicol-induced asplastic anemia.